56 comments:

Q: On the graphs in the reinforcement and striatum lecture, what is being measured in the graphs with 'responses per second' on the y-axis? For example the graph on the puzzling dissociation between liking and reinforcing?

A:In the reinforcement studies examining drug taking, and in the graph dissociating liking and wanting, responses per second are the number of times the participant (rat/human) makes a lever press or button press to receive more of the drug. The figure shows that as people press for the drug at low doses they do NOT rate themselves as liking the drug very much (rated by a scale). At higher doses they now continue to press the same amount to obtain the drug (i.e. they still want it as much), but now rate themselves as liking the drug.

"The format is different to last years exams, because we only do 2 essays, do we only have 6 to choose from or is it still 9?"

Answer: Its 2 from 6.Within the 3 hour exam the first section is 50 MCQs (roughly 2 per lecture), the second section requires you to choose 2 questions from 6 options. These are chosen randomly across the course. Some questions bridge over several lectures.

Is the current consensus regarding how we form memories that the hippocampus is vital for forming declarative memories through LTP?

A: There is a general view that LTP may be core component of memory. It is generally assumed to be the mechanism by which patterns of cells become 'wired' togehter. There is evidence that if you block LT,P or prevent it, learning is impaired. However, not everyone agrees and the process is likely to be more complex.

Please can you explain how the slides on ‘place cells’ link to the rest of the lecture?

A:Good question. Place cells were included in two lectures on the course. This is because they have become a model for understanding the brain's memory sytem, complex processing, and the general functioning of the hippocampus.

The link between LTP and Place cells is that they show the same long-term changes in response to particular stimuli and the same specificity (see Lever et al, 2002 Nature).

Importantly genetically altered mice with distupted LTP show impaired stability of their place fields compared to normal mice. This implies that while normal animals can learn to recognise the same place each time they enter it, genetically altered mice do not, they are 'amnesic' for the place.

Was the aim of the lecture to outline the historical views about how memories are formed in the brain, the brain regions responsible for memory, an in depth discussion of the anatomy of the hippocampus and how LTP works and place cells? I’m asking this as I find it much easier to process the content of lectures when I can see how it all links together and then think about what types of essay questions may be asked on this topic.Amnesia

A: I will be giving an overview podcast and I will include that sort of material.

Q When discussing topics of controversy, I understand that you were saying that recognition memory is composed of familiarity and recollection, but were you talking about recognition memory interchangeably with episodic memory?

A: This is unfortunately not clear. Recollection is clearly Episodic memory. However, familarity devoid of context might not be, in some peoples definition. Some would say it is epsodic memory if it is familairty for some specific stumuli encountered once. Some authors do not think the distinction Rec. vs Fam. is valid, just varying memory strength (with Rec. high and fam. low). Larry Squire is an example.

Q: Based on the Doors & People Test, were you saying that the hippocampus is essential for recall but not necessarily recognition (as all patients had hippocampal damage but not all failed recall tasks)? If so, what brain structure is important for recognition?

Yes, and the perirhinal cortex is thought to support familarity (search for review by Aggleton and Brown on PubMed

You mentioned in one of your lectures about place cells and seeing into the future. Can you say a bit more about this? The slides say "corresponding brain activity happens before an event happens"; what do they mean by this?

The 'event' refers to walking down a path. Place cells fired in a certain order during the event, because each one likes (fires action potentials) at different part of the path.

The authors recorded during sleep before the event, i.e. before the rat had ever walked the path. The view of most scientists before this new study was that it would be unrelated to the future path. However, it was not. In sleep before the rat experienced the future path it would walk, the cells were already firing action potentials in the order they would on the path (though this was more a tendency to do this than a highly regular thing). The conclusion is that cells are pre-set up in cell assemblies that get recruited when you experience new events, such that they are not entirely randomly selected, rather some groups, subgroups will get selected.

This is a complex topic to cover at the 2nd year. It was more meant a very recent exciting advance in how we know now it might be possible to tell what your brain will do tomorrow from your sleep (in theory).

The review article by Moser and Moser (shown on the slide) helps clarify I hope.

Lecture 16 (Invertebrate memory, no-audio) discussed Drosophila mutations and the affect each mutation had on the signal transduction cascade.

Can you recommend any papers to read on this/do we need to know how this cascade works?The slides note which mutation affects which part of the cascade but does not explain how/what effect each part has.

Please could you put the full size slides for your vertebrate memory lecture on POS. The version on POS at the moment is set up for slide (6 slides to a page) which is great for printing off but I can't zoom in to read the detail of the diagrams.

1. Can you say a bit more about what we need to take away from the three pathways in the hippocampus?2. I had thought I had understood that LTP was due to pre-synaptic changes resulting in an increase of vesicles containing neurotransmitter. But your slides suggest it could also be a post-synaptic retrograde messenger or additional terminal buttons. Has this been resolved or is the debate ongoing? 3. "seeing the future". This can't actually mean seeing the future can it? The paper says that the firing sequences seen in sleep are then the firing sequences used in reality. A minimal interpretation of this is that the brain has preallocated cell assemblies for the next bit of place memory whatever it is!

The emotion and reward lecture slides from 2011 are yet to go onto POS. Can you please ask the lecturer to put them on? Difficult to revise the lecture content if we don't have access :-)

Also re the MCQ. There are two questions that we are confused on because the answer on the slide is not the same as the answer provided in your sample MCQ.

15 Which of the following is NOT a typical effect of activation of the sympathetic branch of the autonomic nervous system?a) Sweatingb) Flushing <-- our lecture notes say thisc) Elevated heart rated) Pupillary dilation <-- your answer says this

20 Which of the following is NOT true about oxytocin?(a) It is a steroid hormone <-- our lecture say this(b) It is made in the hypothalamus(c) It is released by the posterior pituitary gland(d) It exerts effects via dopamine modulation in the nucleus accumbens <-- your answer says this, but out notes say this is true

Each lecturer submits an exam question to me per topic. I pick the clearest and try to give coverage across the course. This is not possible with 6 options so not all the lecturers will have questions in the exam.

I didn't understand the podcast when it explained the LO localizer- what is happening in the experiment?

For the acquiring memories test- the participant couldn't remember the words apple and hammer, why? Was the participant told during the study period to learn tiger/bus semantically and apple/hammer by looking at the syllabus (or vice versa)?

For the Brown Sequard Syndrome: Why is there loss of tactile, vibration and proprioception sensation on the same side of the lesion and pain temperature loss on the opposite side of the lesion?

eg pathways such as the dorsal column/medial lemniscus pathway which mediates light touch, proprioception and vibration decussate in the medulla, why is the loss of sensation then ipsilateral if one side of the brain controls the opposite side?

I didn't understand the podcast when it explained the LO localizer- what is happening in the experiment?

The localizer scan is used to find a brain area or areas that respond to some specific category. Classic categories are faces and places. In the localizer scan subjects see faces objects and places. The place area responds selectively to Places for example. Once the localised regions are found scientists study what that region does in other experiements, such as watching hollywood movies (Hasson et al., 2004 Science).

For the acquiring memories test- the participant couldn't remember the words apple and hammer, why? Was the participant told during the study period to learn tiger/bus semantically and apple/hammer by looking at the syllabus (or vice versa)?

Go read the paper cited to get a good understanding: Otten et al. 2001 (I think).

The subjects are not warned about their memory being tested they just think its a catogrisation task. This is because humans don't spend most of our time going round trying to memorize things.

Relational binding theory (more recently Binding item to context(BIC) models) tackle the issue of encoding memories for the short term - suggesting the hippocampus specifically bindings items/objects with time and space. Multiple trace theory argues lots of traces get laid down at encoding. MTT says little about the nature of the binding, more that the hippocampal involvement depends on what's being retrieved, e.g. if its visuo-spatial (+ involvement. I suggest you read more by Moscovitch/Nadel for MTT and Eichenbaum for the BIC models.

brain imaging cannot tell if a region is neccessary because it is only correlational. It can show a region is recruited in task (e.g. there is a correlation between the increase in the amount of activity of a region and the onset of a particular task) , but it cannot demonstrate that the region is required. To do that you need to disrupt the region with a lesion or Transcranial magnetic stimulation (TMS). This shows that it is impossible or hard to do the task if you don't have the region.

I have a question about the somatosensory lectures:Are we just meant to know the ascending pathways? (i.e. not the descending pathways)Also, I got really confused with the slides. Is the trigeminal system different from the anterolateral system? And where does the spinotrigeminal system come into this? Which pathways should be know?

I'm not too certain whether I'll be right to say that learning in the striatum by dopamine pathways may be considered associative learning (operant conditioning) whereas learning in the hippocampus by long-term potentiation may be considered non-associative learning (habituation, sensitisation), especially with regards to hippocampal learning/memory. Please verify.

good question. The link between areas and type of conditioning is not simple. We didn't go into a lot of detail on operant vs classical vs non-associative conditioning. The reinforcement learning involving action by the animal/human is operant conditioning. The hippocampus is NOT involved in non-associative conditioning. The hippocampus is not generally thought to be part of a simple conditioning system. However, if you need to condition to place, you need the hippocampus

thanks for reminding me to address the MCQ questions. You are quite right the answers are as you indicate.

15 Which of the following is NOT a typical effect of activation of the sympathetic branch of the autonomic nervous system?a) Sweatingb) Flushing CORRECT ANSc) Elevated heart rated) Pupillary dilation

20 Which of the following is NOT true about oxytocin?(a) It is a steroid hormone CORRECT ANS (b) It is made in the hypothalamus(c) It is released by the posterior pituitary gland(d) It exerts effects via dopamine modulation in the nucleus accumbens

The word document file these are in has been updated on POS. I will e-mail all students about this.

Please can you confirm the findings of the delayed discounting task in the reinforcement lecture – was it that there was more activity in the ventral striatum when people opted for less money immediately and this shows that the VTA is associated with a preference for immediate reward?

the dorsal column/lemniscal pathway and theanterolateral pathway both decussate. So why do the patients withBrown-Sequard Syndrome loose the tactile, vibration and proprioceptionsensation from the same side of the lesion and loose on pain andtemperature sensation form the opposite side of the lesion?

The patients with the Brown-Sequard Syndrome suffer from an INCOMPLETEspinal cord lesion. Which means that if there is a partial cut of thespinal cord some fibers will be lesioned and other will not.

If you look at the anatomy of both dorsal column and anterolateral pathway(if you have the slides of the class, the one that has this heading "thesomatosensory information travels to the brain through two pathways"), youwill see that the fibers in the dorsal column/medial lemniscal pathwaydecussate further up, on the dorsal column nuclei: the gracil and thecuneatus. So say information from the left side of the body, will travelthrough the left side until they reach the dorsal column nuclei where theydecussate to the right side.

What happens with the anterolateral pathway? Fibers from the dorsal rootganglion synapse in the dorsal horn and fibers then decussate to the otherside.

This means that a left partial lesion of the spinal cord will cut thefibers of one side and not of the other. At the spinal cord level, fibersfrom the same side of the lesion would cut anterolateral fibers that carryinformation of the right side of the body and dorsal column/lemiscalpathway that carry information from the left side of the body.

Hi,I have a question re the cicadian clock lecture;where do the positive elements come from in the first place? The negative one (or atleast per) comes from the light input, but I can't seem to find where we get the positive elemants that instigate the mRNA transcription in the first place?Thanks guys!

Hi,Just a quick question regarding the format of the exam.For the MCQ section, do we need to know details of each lecture (ie know the stuff in the readings) or are the lecture slides enough? Will there be questions that ask things about readings, or are all the questions asked from stuff on the lecture slides?Thanks

I have a collection of questions that I will present to you in a structured way.

Hemispheric Dominance:

1) Is there any classic research about the dominance of hemispheres, i.e. the overall functional organisation between different people, say left-handed ones and right-handed ones?

2) Are left-handed people on average more intelligent? Any evidence for/against that?

Phineas Gage:

1) Was his intelligence also altered? Did he become smarter or less so? What is the name of the original paper published about him and which subsequent papers are worth reading?

Neuronal Development/Functions:

1) What are the regions of the brain, that is in the brain, which produce in principle new neurons even during adulthood? Are there any classic papers on this issue?

2) Is it possible nowadays to actually observe the default state of the brain? By that I mean the state and activity of the brain during rest while no task is being performed.

3) When speaking of serotonergic, dopaminergic, adrenalinergic and cholinergic projections from certain nuclei in the brainstem, does it mean that those nuclei really actually send neuromodulators/-transmitters to the post-synaptic neurons? Or is it rather that they themselves are receiving such transmitters?

4) What really matters for the dimensions of the brain in terms of the associated intelligence? Is it the ratio? I once came across a paper that states that even the ratio is irrelevant.

5) What happens exactly when the corpus callosum is cut in normal adult subjects. I never understood this.

Last question:

Would it make sense to ask about how our brain might develop in the future? I mean are we in any position whatsoever to claim to be able to project how the evolution of our species might take its course with all the knowledge that we have about ourselves and other animals and the external world?

Hi Hugo,Just wondering if the .05 significance level used in the rest of psychology is standardly used in fMRI studies? I read brain imaging usually maps around 100,000 voxels, so I would have thought there would be a want to be a bit more certain, especially with the cost of running equipment etc.